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oral cavity - BDS 1 > histopathology of caries :) > Flashcards

histopathology of caries :) Flashcards

1
Q

clincial types of cariees

A

acute
chronic
arrested

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2
Q

what is acute caries

A

caries which is extensive

affects flat surfaces of the teeth (ie front of incisors)

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3
Q

what is chronic caries

A

occlusal caries

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4
Q

what is arrested caries

A

caries has stopped due to a change in environment

part of the mouth has become self cleaning

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5
Q

what does ground sectons allow us to look at

A

hard parts of the tooth

cannot preserve soft tissue

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6
Q

demineralised sections

A

organic matrix left

cannot see enamel

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7
Q

normal enamel

A 
prisms
prism borders
cross striations
straie of retizus
surface zone
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8
Q

straie of retizus

A

more pronounced incremental lines

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9
Q

what causes incremental lines

A

ameloblasts stop and rest and then move in a different direction

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10
Q

where does demineralisation generally start and why

A

prism borders
cross straitions
straie of retizus
- have more organic matrix allowing acid to enter

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11
Q

sites for caries

A

smooth surface
fissur
root/cementum
recurrent (caries under a restoration)

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12
Q

types of arrested caries

A

type 1 and type 2

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13
Q

what is type 1 arrested caries

A

advanced dentine lesion becomes self cleaning

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14
Q

what is type 2 arrested caries

A

white spot enamel lesion may remineralise

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15
Q

where does root/cementum caries usually start

A

ACJ - where enamel meets cementum

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16
Q

where is root caries seen

A

proximal and buccal root surfaces

can have multiple lesions on same tooth

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17
Q

caries on cemntum/dentine

A

poorly resistance
PDL fibres allow rapid spread to dentine
caries will progress apically due to tubules in dentine

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18
Q

classifications of pulp pathology

A

inflammatory

degenerative

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19
Q

what is inflammatory pulp pathology

A

pulpitis ie pulp inflammtio

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20
Q

types of degenerative pulp pathology

A

fibrosis
calcifications
internal resorption

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21
Q

forms of pulpitis

A

acute
chronic
then within these are open and closed

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22
Q

what is open pulpitis

A

pulp is open to orla envionrment

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23
Q

what is closed pulpitis

A

enamel is still in tact, pulp not exposed

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24
Q

causes of pulpitis

A 
infection
-dental caries
- cracked teeth
- transient bacteriamia
trauma
physcial, mechanical, chemical
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25
Q

what happens is the pulp is not treated

A

die by necrosis

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26
Q

what happens after the pulp begins to die by necrosis

A

inflammatory process starts at the apex of the root

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27
Q

types of periapicla pathology

A 
periapical periodontis (inflammatory)
reactive
- hypercementosis
- ankylosis
- osteoscelrosis
28
Q

causes of periapical pathology

A

infection (vie root canal, periodontium or bacteriamia)

trauma (chemical, physical, mechanical)

29
Q

what can pulpitis least to

A

formation of a cyst

30
Q

what is the earliest evidence of a carious lesion on a smooth surface

A

white/brown spot

31
Q

where is a lesion most likey to form on a premolar tooth

A

below the contact point between teeth where palaque can stagnante and collect

32
Q

why may lesions be brown instead of white

A

enamel increases in porosity and then pigment of food wll be absorbed

33
Q

how can an early carious lesion be fixefd

A

enamel is still in tact and can be remineralsied

  • removal of plawue
  • apply fluride
  • improve OH
34
Q

what can happen at the ADJ

A

laterla spread of caires

acid can spread more easily

35
Q

what 4 zones are there within the enamel lesion

A

translucent zone
dark zone
body of lesion
surface zone

36
Q

what is the largest zone in the enamel lesion

A

body of lesion

37
Q

what do the zones relate to

A

enamel porisity

38
Q

what zone has the greatest porosity

A

body

39
Q

what porosity results in cavitation

A

20-25%

body can no longer support the surface lesion

40
Q

how does porosity increase

A

movement of calcium out of the tooth

hydroxyapitite mineral is being dissolved out of the enamel

41
Q

translucent zone

A

advancing edge of lesion
small number of large pores
demineralisation at the edgeof prisms
in 50%of lesions

42
Q

dark zone

A 
85-85% lesions
varible in thickness 
narrower =more rapid advance
more pores but smaller than TZ
represents re-precipitation of minerals dissolved out in TZ
43
Q

body of lesion

A

demineralisatio of prism cores
pore volume 20% centre 5% edge
some amount of reprecipitation

44
Q

surface zone

A

unaffected layer
incontact with surface biofilm
resisits demineralisation until dentine involved

45
Q

dynamic process of de/remineralsiation

A

acid influxes results into demineralisation and movement of CA out
fluride favours reminerlisation
(calcium moves in)

46
Q

earliest clinical evidence in enamel fissure caries

A

white opacit around fissure paerure

may be sticky brown spot

47
Q

shape of fissure caries and where do they arise and spread

A

conical lesion with base towards ADJ
lesion arise in fissure walls
spread at ADJ

48
Q

how does fissure caries progress into dentine (types)

A 
priamry enamel caries
- lateral spread at ADJ
secondary enamel caries
- careis extends backwards
early dentine caries 
- acid diffuses to dentine
49
Q

what respond toether as a compelx

A

dentine and pulp

50
Q

how does the dentine and pulp respond to caries

A

dentine tubules run from ADJ to the pulp

the tubules are closed off in responce

51
Q

what are defence reactons of plaque acid

A

tertiary dentine
scelrotic entine
dead tracts

52
Q

tertiary dentine

A

closes off the tubules at the pulp end and make more dentine

53
Q

sclerotic dentien

A

fill in the tubules

mineralisation of odontoblast processes

54
Q

dead tracts

A

empty tubules sealed at th end and filled with air

odontoblast death

55
Q

what the the shapeof caries affected by

A

site

ie fissure vs smooth surface

56
Q

dental caries before cavitation

A

acid diffuses through intact porous enamel

pulp dentine unit repspods

57
Q

what are the two main zones before cavitation

A 
scelortic zone (around the outside)
body of lesion (deminerlised)
58
Q

how does cavitation occur

A

surface enamel no longer able to structurally support itself

(carious enamel collapses_

59
Q

what happens after bactera has entered the dentine

A

1st wave - aidogenic bactera enter, demineralise enamel and dentine
2nd wave
colonisation of different bacteria
mixed popilation produce proteolytic enzymes that destroy demineralisaed collagen matrix

60
Q

what do bacteria do in the dentine tubules

A

mulitply in the tubules which widen and collapse

‘liquefaction foci’

61
Q

what does collapsing of dentine tubles lead to

A

expansion and formation of dentine clefts

thes can flake off (point of weakness)

62
Q

what is the body of the lesion subdivied into

A

demineralisation
bacterial penetration
destruction

63
Q

what is in the demineralisation part of the body of the cavitation

A

dentine has lost mineral but still has tubular structure

no bacteria and dentine is stained

64
Q

what is in the bacteria penetration of the body

A

bacteria multiply in tubles
infected soft dentine
stil maintains some tubular matrix

65
Q

describe the destruction in the body

A

base of cavity
discoloured
liquefaction foci and transverse clefts

66
Q

where is the head of the scleotic zone

A

near the pulp

67
Q

what happens to the pulp upon caries advancing

A

pulp tries to shrink away from caries
odontoblasts wrking hrder to make dentine more quickly
tertiary dentine increasing in irregularity
pulp inflammation increases
bacteria invade tertiary dentine and reach pulp

oral cavity - BDS 1 (66 decks)

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